**8. Neuropsychological assessment for Capgras syndrome**

The term CS does not demonstrate a well-defined mental disorder. Over the years various studies have suggested psychodynamic and neurophysiological interpretations for CS, and various aetiologies have been recommended for the condition's development [15, 17, 28].

Although frequently seen in psychotic cases, Capgras has also been associated with neurological disorders suggesting that the syndrome has an organic basis [14]. According to a study, CS patients were classified into groups according to whether or not they had evidence of neurological disorder. Some of the patients identified as having no neurological lesion might be found to have organic brain disease with more sophisticated imaging techniques or at post-mortem evaluation [41]. In another study, approximately one in five of patients with CS presented with organic mental disorders [1, 2]. Multiple hypotheses have been put forth regarding the underlying pathophysiology of CS. Some areas of the brain are responsible for the etiology of this disease. Results of structural and neuroimaging studies of CS provide support for an organic etiology [17]. Multiple studies and reports have remarked on CS in the setting of various neurological and neurodegenerative diseases [42]. There is a study that found more widespread bilateral frontal and temporal cortex atrophy in schizophrenia patients with CS than schizophrenia patients without the syndrome by using computerized tomography (CT) [17]. Likewise other studies using CT found global brain atrophy in combination with right hemisphere lesions in patients with dementia. There is also reported that positron emission tomography [PET] demonstrated

abnormal brain glucose metabolism in paralimbic structures and temporal lobes of patients with Alzheimer's dementia comorbid with CS and other subcategories of delusional misidentification syndromes [17]. Numerous neuropsychological researches support an association between CS and right frontal and temporal lobe abnormalities, and also many study reports indicate that patients with CS tend to have inferior scores on neuropsychological tests of frontal lobe function [17]. Even though less well documented, regions of the prefrontal cortex are also associated within facial processing: projections from the face processing areas in the right ventromedial occipitotemporal regions to the ventromedial prefrontal cortex via the uncinate fasciculus as well as limbic-thalamic pathways are well established [34].

#### **9. The association between Capgras delusion and schizophrenia**

Some people with schizophrenia exhibit this syndrome, but it is not related directly to schizophrenia itself; there are people with schizophrenia who do not exhibit CS, as well as people with CS who do not exhibit schizophrenia. The mean age of schizophrenic patients with Capgras syndrome is older than the age at which schizophrenia alone is usually expected to occur. When brain abnormalities of people with schizophrenia affect certain areas, CS and schizophrenia will occur concurrently. Capgras delusion and schizophrenia seem to be statistically related, at least in the case of the paranoid subtype of schizophrenia. It has been claimed that right hemisphere damage is a characteristic of schizophrenia; perhaps the imperfect evaluation of beliefs, which we have suggested, occurs as an outcome of damage to a particular area of the right frontal lobe, which is necessary for the occurrence even of the persecutory and grandiose delusions that are common in paranoid schizophrenia. Accounting the association of Capgras delusion with paranoid schizophrenia, the same neuropsychological deterioration of belief assessment is required for both, and in cases of patients with persecutory or grandiose delusions where the neuropathology also has affected the track from face recognition to the autonomic nervous system, Capgras delusion will also be existing [43, 44]. CS in paranoid schizophrenia may improve with successful treatment. But recurrence of illness may be accompanied by a return of delusional material [44].

#### **10. Differential diagnosis of primary and secondary Capgras delusions**

It is important to note that the Capgras delusion can be either a primary condition that is part of a 'mental illness' or a secondary condition that is the direct result of an organic disease of the brain. Also, the primary and secondary versions differ significantly in their presentation. In primary Capgras syndrome, the patient is more likely to be furious or violent toward the imposter. In secondary CS, the imposters do not change over time. This is different from the situation in schizophrenia where the delusions can vary [45]. The mean age of onset of the delusion was earlier in primary Capgras (mean age 32 years) than in secondary Capgras (mean age 48.5 years). Primary cases are more likely to have a subtle onset which evolved gradually, whereas secondary cases are more likely to have sudden-onset delusions. Primary cases show associated psychotic symptoms, particularly paranoid thought, whereas psychotic symptoms are not very often of the secondary cases. The patients with CS without apparent organic cerebral dysfunction were more likely to have experienced other psychiatric symptoms prior to the onset of the Capgras delusion than those with organic cerebral dysfunction [41]. Patients

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*What is Capgras Syndrome? Diagnosis and Treatment Approach*

**11. The role of Capgras syndrome in violence**

**12. Differential diagnosis of Capgras syndrome**

The differential diagnosis of patients who suffered CS is crucial. It is substantial to rule out the presence of brain disease in every patient with Capgras delusion [45].

with neurological impairments were more likely to regard the misidentification as benign or as due to illusory, whereas patients without evidence of neurological basis were more likely to appraise the delusions as being threatening [41]. Thus, hostility and violence are seen much more frequently in those patients diagnosed as schizo-

Acting on delusions is a crucial clinical issue. There is a positive relationship between delusions and serious violent acts. Although the pathway from delusions to violent outcomes is not direct, the risk is greatly increased when symptoms are acute, especially at the time of initial presentation and if not treated [19]. And the risk also can be changed according to the etiology of delusions. There is a requirement to be concerned about the patient's tendency for violence and to evaluate for it thoroughly in Capgras delusion [45]. In patients with CS of an organic nature, violence may be associated with few or no affective manifestations (e.g., hostility, aggression, and auditory hallucinations), and may not be associated with paranoid elements [7]. Delusional symptoms in CS such as persecutory thoughts, threatcontrol symptoms, command auditory and/or visual hallucinations, and hallucinations of threatening content have all demonstrated to be significant predictors of violence act and aggressive behaviour [28]. If the patients are married, divorced, or separated, the most frequent doubles are the spouse. If the patients are single, the most frequent doubles are the siblings [19]. It should be noted that healthcare professionals may become the objects of delusional misidentification [42]. Because the double is usually assumed to have malicious, the CS could be characterized by hostility toward misidentified objects, and, later, it can lead to physical harm to others [19]. The assault associated with CS, the tendency to violence, cannot be attributed purely to the delusion's existence. Other factors are presumably to affect the possibility of violent act. A significantly higher tendency for interpersonal violence are men disclosed among male subjects, average age at 40 years old, with a history of aggressive behaviour and substance abuse; social withdrawal prior to the violent act is common, and the violence is usually well planned [19, 21, 22]. Persecutory paranoid motivations have been implicated as a key factor in acts of violence toward family members who constitute the majority of victims in CS [28]. Physical violence was expressed by 58.2% of patients with CS and 62.5% of patients with CS engaged in acts of interpersonal violence toward their close family members and caregivers [21, 22]. Mothers and spouses were the most frequently attacked group of relatives, respectively. Also, it was found that 1 of 10 Capgras patients attempted homicide [21, 22]. Most of the perpetrators were males suffering from mental disorders without organic association. A higher incidence of self-harm and suicide attempts, which is about 1 in 10 of patients with CS, was detected among females even in patients with psychiatric disorders and in patients with neurodegenerative disorders [21, 22]. Although in the usual cases, the misidentified object is a person, hence justifying the title of delusional identification of people, the CS is not restricted to person misidentification but can also involve other living or lifeless objects [7, 19]. Physical violence against objects was also common, such as setting fire to one else's estate [21, 22].

*DOI: http://dx.doi.org/10.5772/intechopen.91153*

phrenic than in other patients [46].

*Anxiety Disorders - The New Achievements*

established [34].

abnormal brain glucose metabolism in paralimbic structures and temporal lobes of patients with Alzheimer's dementia comorbid with CS and other subcategories of delusional misidentification syndromes [17]. Numerous neuropsychological researches support an association between CS and right frontal and temporal lobe abnormalities, and also many study reports indicate that patients with CS tend to have inferior scores on neuropsychological tests of frontal lobe function [17]. Even though less well documented, regions of the prefrontal cortex are also associated within facial processing: projections from the face processing areas in the right ventromedial occipitotemporal regions to the ventromedial prefrontal cortex via the uncinate fasciculus as well as limbic-thalamic pathways are well

**9. The association between Capgras delusion and schizophrenia**

illness may be accompanied by a return of delusional material [44].

**10. Differential diagnosis of primary and secondary Capgras delusions**

tion that is part of a 'mental illness' or a secondary condition that is the direct result of an organic disease of the brain. Also, the primary and secondary versions differ significantly in their presentation. In primary Capgras syndrome, the patient is more likely to be furious or violent toward the imposter. In secondary CS, the imposters do not change over time. This is different from the situation in schizophrenia where the delusions can vary [45]. The mean age of onset of the delusion was earlier in primary Capgras (mean age 32 years) than in secondary Capgras (mean age 48.5 years). Primary cases are more likely to have a subtle onset which evolved gradually, whereas secondary cases are more likely to have sudden-onset delusions. Primary cases show associated psychotic symptoms, particularly paranoid thought, whereas psychotic symptoms are not very often of the secondary cases. The patients with CS without apparent organic cerebral dysfunction were more likely to have experienced other psychiatric symptoms prior to the onset of the Capgras delusion than those with organic cerebral dysfunction [41]. Patients

It is important to note that the Capgras delusion can be either a primary condi-

Some people with schizophrenia exhibit this syndrome, but it is not related directly to schizophrenia itself; there are people with schizophrenia who do not exhibit CS, as well as people with CS who do not exhibit schizophrenia. The mean age of schizophrenic patients with Capgras syndrome is older than the age at which schizophrenia alone is usually expected to occur. When brain abnormalities of people with schizophrenia affect certain areas, CS and schizophrenia will occur concurrently. Capgras delusion and schizophrenia seem to be statistically related, at least in the case of the paranoid subtype of schizophrenia. It has been claimed that right hemisphere damage is a characteristic of schizophrenia; perhaps the imperfect evaluation of beliefs, which we have suggested, occurs as an outcome of damage to a particular area of the right frontal lobe, which is necessary for the occurrence even of the persecutory and grandiose delusions that are common in paranoid schizophrenia. Accounting the association of Capgras delusion with paranoid schizophrenia, the same neuropsychological deterioration of belief assessment is required for both, and in cases of patients with persecutory or grandiose delusions where the neuropathology also has affected the track from face recognition to the autonomic nervous system, Capgras delusion will also be existing [43, 44]. CS in paranoid schizophrenia may improve with successful treatment. But recurrence of

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with neurological impairments were more likely to regard the misidentification as benign or as due to illusory, whereas patients without evidence of neurological basis were more likely to appraise the delusions as being threatening [41]. Thus, hostility and violence are seen much more frequently in those patients diagnosed as schizophrenic than in other patients [46].
